Influence of Acute Epinephrine Infusion on Endotoxin-Induced Parameters of Heart Rate Variability

Jan, Badar U.; Coyle, Susette M.; Oikawa, Leo O.; Lu, Shou‐En; Calvano, Steve E.; Lehrer, Paul M.; Lowry, Stephen F.

doi:10.1097/sla.0b013e3181a40193

Cited by 54 publications

(71 citation statements)

References 72 publications

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“…6E. Figure 7 shows how LF and HF both decrease while the LF/HF ratio increases, in agreement with experimental data (28,35,36). The Poincaré maps displayed in Fig.…”

Section: Resultssupporting

confidence: 77%

“…In human endotoxemia, HF and LF power both decrease acutely before recovering (28,35,36). Both circadian and acute responses may be explained by the link between vagal activity and HF and LF oscillations.…”

Section: Methodsmentioning

confidence: 99%

“…Then, the peaks in the power spectrum fall directly within the HF and LF bands, facilitating the use of standard methods of calculating HF and LF power to study model output. The amplitudes of the HF and LF sinusoids depend on T par, which produces homeostatic circadian rhythms in HRV (33,43,53) as well as acute suppression of HRV in endotoxemia (28,35,36).…”

Section: Methodsmentioning

confidence: 99%

“…Responses observed in human endotoxemia experiments mimic observed responses in systemic inflammation in ICU patients, albeit over different timescales (30), thus making the human endotoxemia model an excellent platform for exploring mechanistic underpinnings of the systemic inflammatory response. A key component in the response to endotoxemia is a decrease in HRV, concomitant with imbalances in autonomic activity reflected by perturbed autonomic oscillatory responses in heart rate (HR) (28,35,36,65).Despite an understanding of the importance of inflammation in a wide variety of disorders and a large number of experiments elucidating the details of the inflammatory response, novel treatments aimed at controlling inflammation remain elusive (25). The complexity of the interacting, redundant pathways involved in the inflammatory response necessitates a systems-level understanding of inflammation (72,80), thus leading to interest in the inflammatory response from a systems biology perspective (79).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

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Modeling autonomic regulation of cardiac function and heart rate variability in human endotoxemia

Scheff¹,

Mavroudis

Calvano

et al. 2011

Physiological Genomics

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Scheff JD, Mavroudis PD, Calvano SE, Lowry SF, Androulakis IP. Modeling autonomic regulation of cardiac function and heart rate variability in human endotoxemia. Physiol Genomics 43: 951-964, 2011. First published June 14, 2011 doi:10.1152/physiolgenomics.00040.2011.-Heart rate variability (HRV), the quantification of beat-to-beat variability, has been studied as a potential prognostic marker in inflammatory diseases such as sepsis. HRV normally reflects significant levels of variability in homeostasis, which can be lost under stress. Much effort has been placed in interpreting HRV from the perspective of quantitatively understanding how stressors alter HRV dynamics, but the molecular and cellular mechanisms that give rise to both homeostatic HRV and changes in HRV have received less focus. Here, we develop a mathematical model of human endotoxemia that incorporates the oscillatory signals giving rise to HRV and their signal transduction to the heart. Connections between processes at the cellular, molecular, and neural levels are quantitatively linked to HRV. Rhythmic signals representing autonomic oscillations and circadian rhythms converge to modulate the pattern of heartbeats, and the effects of these oscillators are diminished in the acute endotoxemia response. Based on the semimechanistic model developed herein, homeostatic and acute stress responses of HRV are studied in terms of these oscillatory signals. Understanding the loss of HRV in endotoxemia serves as a step toward understanding changes in HRV observed clinically through translational applications of systems biology based on the relationship between biological processes and clinical outcomes. systems biology; inflammation; circadian HEART RATE VARIABILITY (HRV) is generally defined as the quantification of the distribution of time intervals between successive heartbeats. Reduction in HRV, a manifestation of altered autonomic function under stress, is potentially a useful predictor of outcome in myocardial infarction (42), congestive heart failure (63), diabetic neuropathy (58), and neonatal sepsis (46). Diminished HRV has also been observed in critically ill patients in intensive care units (ICU) (52), which motivates interest in HRV as a critical variable in the recovery from critical illness (50). Due to this clinical relevance, dynamic characteristics of HRV have been assessed by time domain, frequency domain (76), and nonlinear metrics (46, 60). The majority of HRV research has thus far focused on the interpretation of the patterns of HRV (45) rather than linking cellular-level mechanisms to patterns (11). The realization that health may be characterized by a certain degree of variability of human heart signals motivates the hypothesis that appropriate physiological variability is the manifestation of robust dynamics of control signals whose fluctuations equip the host with the ability to anticipate external and internal disturbances. We hypothesize that these variable dynamics are driven by the convergence of rhythmic physiological signals on...

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“…6E. Figure 7 shows how LF and HF both decrease while the LF/HF ratio increases, in agreement with experimental data (28,35,36). The Poincaré maps displayed in Fig.…”

Section: Resultssupporting

confidence: 77%

Section: Methodsmentioning

confidence: 99%